ArticleBMC microbiology2008
The influence of in vitro fitness defects on pneumococcal ability to colonize and to cause invasive disease.
Article in BMC microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
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- Targeted control of pneumolysin production by a mobile genetic element inMicrobial genomics · 2022Article
- The Role of the Universally Conserved ATPase YchF/Ola1 in Translation Regulation during Cellular Stress.Microorganisms · 2021Review
- Prophage Excision inFrontiers in microbiology · 2019Article
- Spectrum of antibacterial activity and mode of action of a novel tris-stilbene bacteriostatic compound.Scientific reports · 2018Article
- Histidine 114 Is Critical for ATP Hydrolysis by the Universally Conserved ATPase YchF.The Journal of biological chemistry · 2015Article
- Genetic factors regulating lung vasculature and immune cell functions associate with resistance to pneumococcal infection.PloS one · 2014Article
- A universally conserved ATPase regulates the oxidative stress response in Escherichia coli.The Journal of biological chemistry · 2012Article
- Intrinsic epidemicity of Streptococcus pneumoniae depends on strain serotype and antibiotic susceptibility pattern.Antimicrobial agents and chemotherapy · 2011Article
- International pneumococcal clones match or exceed the fitness of other strains despite the accumulation of antibiotic resistance.Antimicrobial agents and chemotherapy · 2011Article
- The universally conserved prokaryotic GTPases.Microbiology and molecular biology reviews : MMBR · 2011Review
- Compensation of fitness costs and reversibility of antibiotic resistance mutations.Antimicrobial agents and chemotherapy · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStreptococcus pneumoniae is a genetically diverse major human pathogen, yet a common colonizer of the nasopharynx. Here we analyzed the influence of defects affecting in vitro growth rate, on the ability of S. pneumoniae to colonize and to cause invasive disease in vivo.
resultsOf eleven different clinical isolates one serotype 14 carrier isolate showed a significantly longer generation time as compared to other isolates, and was severely attenuated in mice. To directly investigate the impact of growth rate on virulence, a panel of mutants in five non-essential housekeeping genes was constructed in the virulent TIGR4 background by insertion-deletion mutagenesis. Three of these mutants (ychF, hemK and yebC) were, to different degrees, growth defective, and showed a reduced invasiveness in an intranasal murine challenge model that correlated to their in vitro growth rate, but remained capable of colonizing the upper airways. The growth defect, as well as virulence defect of the hemK insertion-deletion mutant, was mediated by polarity effects on the downstream yrdC gene, encoding a probable chaperone in ribosome assembly.
conclusionWe conclude that large fitness defects are needed to completely prevent pneumococci from causing invasive disease after intranasal challenge. However, even severe growth defects still allow pneumococci to persistently colonize the upper airways.
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